What are the types of premature ventricular contractions (PVCs)?

Types of Premature Ventricular Contractions

PVCs are classified by anatomical origin, morphology, frequency pattern, and underlying substrate—distinctions that directly determine prognosis and guide ablation strategy.

Classification by Anatomical Origin

Right Ventricular Outflow Tract (RVOT) PVCs

• RVOT PVCs display left bundle branch block (LBBB) morphology with inferior axis (dominant R waves in leads II, III, aVF) and are the most common idiopathic form, typically benign in structurally normal hearts 1, 2.
• These PVCs show smaller R-wave amplitudes in precordial leads V1-V6 and larger S-wave amplitudes in V1-V3 compared to left-sided origins 2.
• RVOT PVCs have longer coupling intervals (358±37 ms) and wider QRS duration (145±13 ms) than Purkinje-origin PVCs 3.

Left Ventricular Outflow Tract (LVOT) PVCs

• LVOT-aortic sinus cusp PVCs present with LBBB morphology but significantly larger R-wave amplitudes in leads II, III, and aVF compared to RVOT origins 2.
• An R-S difference index (V2R + V3R + V4R - V1S) >20.9 predicts LVOT origin with 73.7% sensitivity and 86.3% specificity 2.

Purkinje Network PVCs

• Right Purkinje PVCs demonstrate LBBB with superior axis, while left Purkinje PVCs show right bundle branch block (RBBB) morphology 3.
• These are characterized by shorter QRS duration (126±18 ms) and markedly shorter coupling intervals (292±45 ms) compared to outflow tract PVCs 3.
• Purkinje PVCs are more likely to trigger ventricular fibrillation during electrical storms (18±28 episodes vs 5±5 for RVOT) and require urgent ablation 3.

Classification by Morphology and Complexity

Unifocal vs. Multifocal PVCs

• Multifocal PVCs (≥2 distinct morphologies) indicate higher risk and are associated with increased death, stroke, and cardiovascular events even without sustained VT 4.
• Multifocal PVCs predict presence of myocardial fibrotic substrate on cardiac MRI (P=0.01), requiring pre-ablation imaging 5.

Monomorphic vs. Polymorphic Patterns

• Monomorphic PVCs maintain stable single QRS morphology beat-to-beat, typically originating from a single focus 1.
• Polymorphic patterns suggest multiple foci or underlying structural disease requiring comprehensive evaluation 1.

Bidirectional Ventricular Tachycardia

• Beat-to-beat alternation in QRS frontal plane axis, classically seen with digitalis toxicity or catecholaminergic polymorphic VT 1.

Classification by Frequency and Burden

Low-Burden PVCs (<10% of total beats)

• Generally benign in structurally normal hearts, requiring only reassurance and avoidance of triggers 6, 7.
• Present in approximately 50% of all people with or without heart disease on prolonged monitoring 1, 6.

Intermediate-Burden PVCs (10-15% of total beats)

• Require closer echocardiographic surveillance every 6-12 months due to emerging cardiomyopathy risk 6, 7.

High-Burden PVCs (>15-20% of total beats)

• Independently associated with PVC-induced cardiomyopathy and warrant aggressive management with catheter ablation as primary therapy 4, 6.
• PVC burden ≥24% is independently linked to cardiomyopathy development 7.

Classification by Underlying Substrate

Idiopathic PVCs

• Occur in structurally normal hearts without identifiable cause, most commonly from RVOT with characteristic LBBB morphology and inferior axis 4.
• Suppress with exercise in benign cases, distinguishing them from pathologic substrates 7.

Ischemic PVCs

• Leading cause in older patients, associated with increased mortality risk particularly post-MI with LVEF <35% 4.
• Frequent or prolonged ventricular ectopy during acute coronary syndrome signals incomplete revascularization and warrants immediate angiography 6.

Substrate-Related PVCs

• RBBB morphology PVCs predict fibrotic substrate on CMR (P<0.001), requiring pre-ablation imaging to guide strategy 5.
• QRS duration >160 ms with LBBB morphology may signal early arrhythmogenic right ventricular cardiomyopathy 7.

Classification by Coupling Pattern

Short-Coupled PVCs (<300 ms)

• High-risk feature requiring aggressive management, associated with increased arrhythmia vulnerability 6.
• Purkinje-origin PVCs triggering VF demonstrate coupling intervals of 292±45 ms 3.

Long-Coupled PVCs

• Typical of RVOT origins (358±37 ms), generally more benign when isolated 3.

Critical Clinical Distinctions

The most important prognostic distinction is not PVC morphology itself but the presence of underlying structural heart disease 4, 8. Risk stratification requires:

• 24-hour Holter monitoring to quantify burden (≥2,000 PVCs/24h associated with 30% prevalence of structural disease) 7.
• Echocardiography mandatory for burden ≥24% to assess for cardiomyopathy 7.
• Cardiac MRI with contrast indicated for RBBB morphology, multiple morphologies, or burden ≥2,000/24h to identify fibrotic substrate 7, 5.
• Exercise stress testing to assess PVC behavior (suppression = benign; increase = pathologic) 7.